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Clinical Investigations: ASTHMA |

Racial Differences in Physiologic Parameters Related to Asthma Among Middle-class Children* FREE TO VIEW

Christine L. M. Joseph, PhD; Dennis R. Ownby, MD; Edward L. Peterson, PhD; Christine C. Johnson, PhD
Author and Funding Information

*From the Henry Ford Health System (Drs. Joseph, Peterson, and Johnson), Detroit, MI; and Medical College of Georgia (Dr. Ownby), Augusta, GA.

Correspondence to: Christine L. M. Joseph, MD, Henry Ford Health System, Department of Biostatistics & Research Epidemiology, 1 Ford Place, 3E, Detroit, MI 48202



Chest. 2000;117(5):1336-1344. doi:10.1378/chest.117.5.1336
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Background: Asthma morbidity and mortality are higher in the United States for African-American (AA) children when compared to European-American (EA) children.

Study objectives: To explore racial differences in physiologic factors associated with pediatric asthma severity.

Design: Cross-sectional.

Methods: We analyzed data from two groups of children in suburban Detroit, one of which contains non-urban, middle-class AA children, a group not usually included in childhood asthma studies. All children were 6 to 8 years of age. Clinical evaluations included medical history, physical examination, skin testing, spirometry, and methacholine challenge.

Results: The study population (n = 569) was 14% African American, 51% of the participants were male, and the mean age was 6.8 ± 0.4 years. Socioeconomic status (parental education) was similar overall by race, although some strata-specific differences were observed. The prevalence of physician-diagnosed asthma was 10% for both AA and EA groups. AA children were more reactive to methacholine than EA children (42% vs 22%, respectively; p = 0.001), and had significantly higher total IgE than EA children (geometric mean, 60.6 vs 27.5 IU/mL; p = 0.001). Serum IgE was related to methacholine reactivity in EA children (p = 0.001), but not AA children (p = 0.73). These differences remained after adjustment for gender, age, parental education, parental smoking, and maternal smoking during pregnancy.

Conclusions: Our data support previous reports of racial differences in lung volume, airway responsiveness, and serum IgE concentrations. We found a racial difference in the relationship between total serum IgE and airway responsiveness that is unreported elsewhere. Overall, our results suggest that AA children may be predisposed to asthma.

Figures in this Article

Asthma is recognized in the United States and other industrialized countries as the most common chronic disease of children.110 In this country, morbidity from asthma is greater in African-American (AA) children compared to European-American (EA) children.14 AA children have higher rates of emergency department utilization and hospitalization due to asthma, and mortality from asthma has been higher for AA subjects in comparison to other racial groups since the mid-1980s.510

The observed racial differences in asthma morbidity and mortality may reflect a difference in disease severity. Assessing differences in asthma severity is difficult since commonly used measures of severity (eg, number of emergency department visits, hospitalizations, asthma medications used, etc.) are highly influenced by social and economic factors, such as access to health care, quality of health care, referral to specialists, and health care seeking behavior.1114 Alternatively, asthma severity can be assessed utilizing immunologic or physiologic variables. Although no single measure can determine the severity of asthma, measures of airway obstruction, airway responsiveness, total serum IgE, and allergen sensitization have been shown to be related.1516

Previous studies addressing racial differences in asthma severity have left many unanswered questions. Most previous studies have focused on low-income, urban African Americans, albeit due to the increased morbidity observed in these populations, but it has been difficult to separate racial effects from the effects of poverty. The objective of this study was to examine immunologic and physiologic variables related to asthma severity in AA and EA children of similar socioeconomic status (SES), and residing in the same metropolitan area. By examining these variables in a multiethnic population of middle-class children, we hoped to reduce the confounding effects of SES on racial differences.

Recruitment

The data used in these analyses were from a combination of two study groups of children residing in suburban Detroit, MI: the Childhood Allergy Study (CAS) and Southfield Childhood Allergy Study (SCAS). The selection of the CAS has been previously described.17 Briefly, all pregnant women ≥ 18 years old belonging to the Health Alliance Plan health maintenance organization and residing in a defined group of zip codes encompassing the northern middle-class suburbs of Detroit, MI, were eligible if they had an estimated delivery date between April 15, 1986, and August 31, 1989. Research nurses recruited women during midterm prenatal visits. Only one child per family was eligible for enrollment in the study. Race was classified according to the self-report of the mother. Between the age of 6 and 7 years, study children were invited to undergo their first clinical evaluation. Because the CAS group had few AA children, a second group, the SCAS, of approximately the same age, was recruited from within the same geographic suburban area to undergo the identical clinical evaluation. Recruitment focused on Southfield, MI, a particular suburb within the CAS study area that has a more multiethnic population. According to the 1990 census, AA residents in Southfield have a SES comparable to that of the parents of the children in the CAS cohort. Children were eligible for study if they were enrolled in first grade as of September, 1996. Schools were approached one at a time until the desired sample size was achieved. Since recruitment occurred within the same area as the CAS, children already participating in the CAS were excluded from participation in the SCAS. After an introductory letter explaining the study, parents of eligible children were contacted by phone by the same research nurse who recruited the CAS children, and a clinic visit was scheduled. If parents were not interested in a clinic assessment, the research nurse still attempted to conduct the telephone interview.

Only children coded as “African American” or “European American” were included in this analysis. Races were combined across the two groups to form the final study population (ie, AA children from SCAS and CAS were combined and compared to a combination of EA children from both groups). Prematurity and low birth weight have been associated with asthma.18 The CAS cohort included only “term births” and children with a birth weight > 2,500 g. To increase comparability, this protocol was expanded to the SCAS cohort, in that children with birth weights < 2,500 g were excluded from all analyses.

Clinic Assessments

The clinical assessments for all children were conducted by the one nurse and two physicians. The series of CAS clinic visits were completed first, followed immediately by clinic visits for the SCAS group. The assessments included the following: a medical history and physical examination, allergen skin testing, spirometry, methacholine challenge (provocative dose of methacholine causing a 20% fall in FEV1 [PD20]), and measurement of total and allergen-specific IgE. An attempt was made to collect a urine specimen during the clinic assessment for measurement of cotinine and creatinine. Skin tests were performed by puncture techniques using commercial (Bayer Pharmaceutical; Spokane, WA) extracts of Dermatophagoides farinae, Dermatophagoides pteronyssinus, cat, dog, Alternaria, short ragweed, and bluegrass, in addition to positive and negative controls of saline solution and histamine (1 mg/mL). A positive skin test was defined as one with a sum of perpendicular wheal diameters ≥ 4 mm with a larger surrounding flare.

Spirometry was performed using a KoKo spirometer (Pulmonary Data Service; Louisville, CO) connected to a personal computer. Predicted values were based on the equations of Polgar and included a racial adjustment of 0.8519. This study focused on FVC and FEV1.

All spirometric assessments were generally performed according to American Thoracic Society standards.20 Spirometry was performed with the children standing and without nose clips. There were two deviations from American Thoracic Society standards. One such deviation occurred when a child could not reproducibly produce maximal peak flows. In these cases, the FEV1 and FVC were given priority and accepted as reproducible if there was < 5% variation in both measures. The second was that some children could not sustain exhalation > 3 s. Since efforts were made to optimize the FEV1 and FVC, these measurements were our primary analytic variables.

Children with initial FEV1 < 70% of predicted were given a bronchodilator (albuterol sulfate by nebulization) and reassessed 15 min later. If a child’s initial FEV1 was > 70% of predicted and three maneuvers were reproducible, the child was sequentially challenged with the normal saline diluent and five doses of methacholine (0.025, 0.25, 2.5, 10, and 25 mg/mL) administered with a DeVilbiss 645 nebulizer (DeVilbiss; Bornemouth; England) connected to a French-Rosenthal dosimeter (PDS Instrumentation; Louisville, CO) integrated into the spirometer. The dosimeter was set to deliver methacholine for 0.6 s at the initiation of inhalation during tidal breathing for five breaths. Spirometry was repeated 3 min after each dose of methacholine. Increasing concentrations of methacholine were administered until FEV1 fell to < 80% of the best postsaline solution value or until the maximum concentration was reached. A positive methacholine challenge was defined as a decrease in FEV1 to < 80% of the postsaline solution value following inhalation of methacholine at concentrations up to 10 mg/mL (66 breath units).

Children were classified as having a medical diagnosis of asthma if the parent reported ever being told by a physician that the child had asthma. Current asthma was defined as a physician’s diagnosis of asthma and a report of asthma symptoms in the last 12 months.

Laboratory Methods

Total and allergen-specific serum IgE concentrations were measured using commercially available assays (AlaSTAT; Diagnostic Products; Los Angeles, CA). Both total and allergen-specific serum IgE concentrations are expressed in international units per milliliter. Values of specific IgE ≥ 0.35 IU/mL were considered evidence of detectable antibody as recommended by the manufacturer. The allergens tested were the same as those listed for skin testing. In addition, the serum of all SCAS children and a random sample of 116 CAS children were tested for cockroach-specific IgE. A random sample of 10% of all samples was repeated for quality-control purposes with> 98% agreement.

Cotinine in the urine was measured by radioimmunoassay by the Clinical Biochemistry Facility, American Health Foundation (Valhalla, NY). Creatinine was also measured to correct for the dilution of the urine. All analyses were performed using the cotinine/creatinine ratio (CCR) as nanograms or cotinine per milligram of creatinine.

Statistical Methods

Comparisons between AA and EA children were done using Student’s t test for continuous variables andχ 2 tests for either nominal or ordinal data. If cell frequencies were very small, a Fisher’s Exact test was used in two-by-two tables. When appropriate, odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were computed. Multiple linear regression techniques were used to assess the relationship between IgE values and airway responsiveness. Logistic regression and analysis of covariance (ANCOVA) were used to assess the relationship between race and other variables while adjusting for potential confounders. A p value < 0.05 was considered to indicate statistical significance.

As expected, IgE values were positively skewed, and were therefore logarithmically transformed prior to analysis to better fit the assumptions of the various statistical tests.21 After analysis, values were retransformed back to the original units.

To express airway responsiveness to methacholine we used an estimate of the methacholine dose-response slope as defined by Le Souef et al.22 This method defines the methacholine slope as follows:

where,

The constant 0.6 was added to make all estimates positive, thus allowing log transformation of the values. The larger the slope, the greater the degree of airway responsiveness to methacholine.

Characteristics of the Study Population

Table 1 shows the enrollment and losses for the individual groups before arriving at the final combined population of 569 (79 AA and 490 EA children). All children were between 6 and 8 years of age at the time of the clinical evaluation. For the CAS group, 601 parents were contacted, of which 80.5% made a clinic visit (Table 1). After applying exclusion criteria for this study, 471 participants (78.4%) were available for analysis. For the SCAS group, a total of 170 children were contacted, 77.1% of which made a clinic visit (Table 1). After applying exclusion criteria for this study, 98 participants (57.7%) were available for study. The difference between the two groups in the percentage available for analysis was mostly due to the exclusion of children with reports of low birth weight from the SCAS group at the time of analysis. Children with a report of low birth weight were excluded from participation in the CAS at recruitment.

The AA children from the SCAS were combined with the AA children from the CAS. Before doing so, we assessed racial differences with respect to selected characteristics. Table 2 shows racial comparisons within each of the two groups that served as the source of the combined population. AA children in the CAS were significantly younger than AA children from the SCAS (Table 2). AA children in the CAS did not differ from the AA children in the SCAS with regard to the proportion of male participants, parental education, parental smoking, or maternal smoking during pregnancy. EA children in the CAS were significantly younger than the EA children in the SCAS (Table 2). In addition, a lower percentage of EA children in the CAS had not finished high school (1.3%), compared to that of EA children from the SCAS (8.0%). No other significant differences between the EA characteristics in the CAS group and the SCAS group were observed.

In the combined population, some differences between AA and EA participants were observed (Table 2). AA children tended to be older by about 8 months (7.5 ± 0.5 years for AA children vs 6.8 ± 0.3 years for EA children), and were less likely to have reports of maternal smoking during pregnancy (2.7% for AA children vs 16.7% for EA children; p = < 0.01).

The prevalence of physician-diagnosed asthma was similar by race (Table 3 ). A lower percentage of AA children met study criteria for current asthma than EA children, although this difference did not reach statistical significance (3.8% vs 6.7%, respectively).

Pulmonary Function

Baseline pulmonary function was successfully performed on almost 99% of participants (Table 3). There was no difference in successful pulmonary function by race. Even after correcting predicted values for racial differences, AA children had significantly smaller FVC and FEV1 values than EA children. The ratio of FEV1 to FVC did not significantly differ by race.

Only 76.9% of AA children had FEV1 ≥ 70% of predicted, compared to 99.2% of EA children (Table 3). Of the children with a baseline FEV1 < 70% predicted, only 1 of 15 AA children responded to albuterol, while 3 of 3 EA children responded (p < 0.01; Table 3).

ANCOVA was used to further assess the racial difference in baseline percent of predicted FEV1. After adjusting for gender, age, education, parental smoking, and maternal smoking during pregnancy, FEV1 remained significantly associated with race, with the racial difference in adjusted mean percent of predicted FEV1 remaining approximately the same (AA children, 75.3 vs EA children, 93.9; p = 0.001).

Methacholine Reactivity

Approximately 24% of all children challenged had a PD20 ≤ 10 mg/mL. AA children were more likely to respond to methacholine at this dose than EA children (41.7% vs 22.3%, respectively; p < 0.01). Considering possible racial differences in the acute response to aβ 2-agonist, we compared the FEV1/FVC ratios of children who had responded by≥ 20% to any dose of methacholine, 15 min after they had received an albuterol nebulization treatment. No racial difference was found (Table 3).

We examined the relationship between race and methacholine reactivity (PD20 ≤ 10 mg/mL vs > 10 mg/mL) in a logistic regression model, adjusting for gender, child age, parental education, parental smoking, and maternal smoking during pregnancy. The adjusted OR for the relationship between race and methacholine reactivity was 2.7 (95% CI, 1.4 to 5.4; p = 0.004). Substituting CCR measurements for reports of parental smoking, the adjusted OR for this relationship was 3.1 (95% CI, 1.5 to 6.4; p = 0.03).

CCRs

The geometric and logarithmic means for the CCR are presented by asthma diagnosis and race in Table 4 . Overall, mean CCR was higher for AA children than for EA children. This trend was observed regardless of asthma diagnosis, although the racial difference among persons with asthma was not significant (NS), and among those without a diagnosis, the p value was 0.05. No statistically significant differences were observed when the geometric mean CCR for children with and without asthma was compared within racial categories, (AA with asthma of 18.92 ng/mg vs AA without asthma of 13.87 ng/mg; p = 0.68; and EA with asthma of 9.58 ng/mg vs EA without asthma of 11.24 ng/mg; p = 0.001).

Serum IgE

There was a significant difference in geometric mean serum IgE in AA compared to EA children, with AA children having higher serum IgE (60.63 IU/mL vs 27.48 IU/mL, respectively; Table 5 ). This difference was also apparent when the percentages of children with serum IgE ≥ 100 IU/mL were compared, 40.6% vs 16.2% for AA and EA children, respectively (data not shown).

For children with asthma, serum IgE level did not differ significantly by race (p = 0.871; Table 5). However, among the children without asthma, AA children had significantly higher IgE than EA children: 59.15 IU/mL vs 24.78 IU/mL, respectively (p = 0.001). When the serum IgE levels for children with and without asthma were compared within racial categories, the difference for AA children was NS (AA children with asthma of 74.44 IU/mL vs AA children without asthma of 59.15 IU/mL; p = 0.68), while the difference for EA children was significant, (EA children with asthma of 67.36 IU/mL vs EA children without asthma of 24.78 IU/mL; p = 0.001).

We examined the relationship between race and geometric mean serum IgE using ANCOVA, adjusting for gender, child age, parental education, parental smoking, and maternal smoking during pregnancy. The adjustment for the covariates accentuated the racial difference in geometric mean serum IgE of 26.8 IU/mL for EA children vs 82.2 IU/mL for AA children (p = 0.001). The ANCOVA was then stratified by physician diagnosis of asthma. Results were similar to that of the bivariate analysis. There was no racial difference observed for children with an asthma diagnosis, (geometric mean serum IgE of 175.3 IU/mL for EA children vs 57.9 IU/mL for AA children; p = 0.246) while a significant difference was again observed for those without asthma (geometric mean serum IgE for AA children of 73.2 IU/mL vs 24.5 IU/mL for EA children; p = 0.001).

We also examined the relationship of serum IgE to methacholine reactivity. As shown in Figure 1 , a significant positive relationship was found between methacholine dose-response slopes and total serum IgE concentrations for EA children, (p = 0.001). This relationship was NS (p = 0.73) for AA children. The slopes of the regression lines for the AA and EA children when compared were not significantly different (p = 0.13). When the analysis was done using PD20 instead of the methacholine dose-response slope, similar results were obtained, in that higher total serum IgE concentrations were significantly associated with lower PD20 values for EA children (p = 0.001), but not for AA children (p = 0.44).

Allergen Sensitization

The prevalence of allergen sensitization by race as assessed by skin test and by allergen-specific serum IgE measurements is shown in Table 6 . Tests for IgE showed that AA children were significantly more likely to be sensitized to ragweed and grass. While the pattern of the skin tests was similar, only the difference for bluegrass was significant. Differences for sensitization to major indoor allergens, including cockroach, did not differ by race.

Our objective was to investigate possible racial variations in immunologic and physiologic parameters associated with asthma severity in young children. In this analysis, we found that the association of serum IgE and methacholine reactivity, widely accepted as a positive one in asthma patients, was not observed in AA subjects. We did find this relationship in the EA children. To our knowledge, this apparent racial difference in the relationship between total IgE and airway reactivity has not been previously reported.15 In addition, we found a racial discrepancy in the magnitude of the difference between serum IgE in asthmatics vs nonasthmatics of the same race.

We conducted our study in a group of middle-class AA and EA children to minimize the confounding effect of SES on the relationships between measures related to asthma severity and race. While racial differences in age and maternal smoking during pregnancy were observed, adjustment for these variables did not dispel the immunologic and physiologic differences found between AA and EA children.

A critical question is the prevalence of asthma in our study compared to other estimates from the United States. The most recent data from the National Health Interview Survey (1993 to 1994) reported a prevalence of asthma symptoms in the preceding 12 months of 7.4% in 5- to 14-year-old children.1 These data were not separated by race within age groups. Previous studies report asthma prevalences from 8 to 14% for children, with urban and minority children being at the higher end of the range.2325 Our 10% prevalence of ever having an asthma diagnosis is consistent with these other estimates, given the methodologic and age differences. The fact that we did not find a higher prevalence of asthma in AA children is partially due to our exclusion of low-birth-weight children. Inclusion of these children from the SCAS group would have increased the AA prevalence from 10.1 to 15% and current asthma from 3.8 to 8%, which are similar to those reported by Crain et al,23 and to the 12.3% prevalence we found in a telephone survey of 8- to 9-year-old children in Southfield.8

We did not observe a positive relationship between methacholine responsiveness and serum IgE in AA children. While failing to find a relationship could be due to the small number of AA subjects, it could also be due to racial differences in the relationship between serum IgE and hyperresponsiveness or asthma. Consistent with the hypothesis of a racial difference is the report by the Collaborative Study on the Genetics of Asthma showing that linkages between chromosomal regions and asthma vary by ethnic group.26

Our findings confirm earlier reports that AA children are significantly more responsive to methacholine than EA children. This relationship was maintained when stratified by parental smoking, the prevalence of which was higher in EA children. It is widely accepted that pulmonary hyperreactivity is a hallmark of asthma, and that greater degrees of hyperreactivity are associated with greater levels of symptoms.27 This may correspond to greater asthma severity among AA children.

We also observed a significant racial difference in total serum IgE. This, too, has been previously reported, but in previous articles, it has been unclear as to whether socioeconomic differences contributed to the difference in serum IgE levels.26 We had anticipated that higher concentrations of total serum IgE would be related to an increased prevalence of IgE specific for common inhalant allergens, especially indoor allergens that have been associated with asthma.28 Racial differences in sensitization were only significant for outdoor allergens. Sensitization to dust mites, cat, dog and cockroach did not differ by race. The differences in the prevalence of sensitization to ragweed and bluegrass are unlikely explanations for the differences in total serum IgE. If environmental factors explained the differences observed, we would expect to see a racial difference in serum specific IgE or in skin test sensitivity for these allergens, and this was not the case. Racial differences in cockroach, Alternaria, and dust mite allergens—all traditionally associated with asthma—were not observed. Racial differences in bluegrass were observed, but this is an allergen not usually associated with clinical asthma on a wide scale. Prevalence of parental report of smoking, another indoor irritant, was actually higher for EA compared to AA children, and although this trend was not observed for CCR, the relationship of race to reactivity remained positive and significant after adjustment for these and other adjunct indicators of tobacco smoke exposure, including maternal smoking during pregnancy.

Few studies regarding asthma have included middle-class AA subjects. This study is one of the first to measure spirometry and methacholine responsiveness in a study sample of AA and EA children of similar SES. It is widely recognized that AA subjects have smaller lung capacities than EA subjects, hence the use of a standardized 15% reduction in the predicted FVC and FEV1 values for AA children. It was surprising to find that even after correction for racial differences, both the average percent predicted FVC and FEV1 were still significantly lower in the AA children. This racial difference in lung volumes is demonstrated by the finding that only 75.9% of AA children had FEV1 ≥ 70% of predicted in contrast to 99.2% of EA children. Study personnel and equipment were the same for all children. The spirometer was calibrated at the start of each day. There was no perceptible difference in the cooperation or effort of the children during spirometry. The difference did not appear to result from subclinical asthma or airway obstruction, since only one of 15 AA children with FEV1 < 70% responded acutely to a bronchodilator, and none of these 15 children had histories suggestive of asthma. Alternative explanations for this difference include the imprecision of an estimate based on the relatively small number of AA children examined, and the possibility that the 15% correction factor is inadequate. A study of AA and EA adults found that the between-subject variability in lung function within a racial group was greater than the difference between races, and suggested that better predictive methods were needed.29 Unfortunately, our data cannot help answer the question of whether smaller lung capacities contribute to more severe asthma.

A potential problem with our study is that we combined two groups of children for analysis. While we feel that the racial differences in the factors we assessed are more likely biological in origin, we cannot totally exclude the possibility of dissimilarity between the two groups, since significant differences in age and parent education were found.

SCAS cohort children averaged about 8 months older than their CAS counterparts. This small differ- ence in age is unlikely to affect our major findings. While serum IgE increases with age, IgE levels do not increase by twofold in a year.30Others have reported that children become less responsive to methacholine as they become older.3132 Thus, any effect of the difference in age between the two groups would probably have led to an underestimate of the effects we have presented.

We also observed a significant difference in the educational attainment of parents for the EA children in CAS vs SCAS groups. Education of the parent is a widely used but imperfect indicator of SES.3334 However, the area from which the second group (SCAS) was drawn is located within the area for recruitment of the initial group (CAS). The objectives of the initial recruitment effort did not include enrollment of a homogeneous group with respect to race; indeed, both African Americans and European Americans were counted among the participants, as were other ethnic groups. To study racial differences, however, the number of AA children in the CAS group was too small. Remaining within that same geographic area, we concentrated our subsequent efforts on neighborhoods we knew to be more racially balanced. Census information from 1990 reports that EA and AA families within the geographic area used for both initial and subsequent recruitment have comparable SES. We note that adjustment for age and parent education did not explain the racial differences observed.

In summary, we found a significant racial difference in the relationship between total serum IgE and airway responsiveness, and between serum IgE and asthma status. To our knowledge, this finding has not been reported in the literature. Our analyses support previously reported racial differences in lung volumes, airway responsiveness, and serum IgE concentrations. These differences are consistent with the hypothesis that AA children may be predisposed to more severe asthma. An alternative hypothesis is that there may be racial differences in factors that predispose to more severe asthma.

More studies of racial differences in factors related to asthma severity are needed with larger populations. Studies of this nature will be instrumental in uncovering the reasons for racial disparities in asthma prevalence and morbidity in this country. Ideal for these assessments would be populations that include large subgroups of major racial classifications, all of which are adequately represented at varying levels of SES.

Abbreviations: AA = African-American; ANCOVA = analysis of covariance; CAS = Childhood Allergy Study; CCR = cotinine/creatinine ratio; CI = confidence interval; EA = European-American; NS = not significant; OR = odds ratio; PD20 = provocative dose of methacholine causing a 20% fall in FEV1; SCAS = Southfield Childhood Allergy Study; SES = socioeconomic status

This study was funded by a Fellowship from the National Heart, Lung, and Blood Institute and the National Institute of Allergy and Immunologic Diseases of the National Institutes of Health (Grant AI24156), and by the Henry Ford Health System Medical Treatment Effectiveness Programs (MEDTEP) Research Center on Minority Populations, through Grant U01 HS07386 from the Agency for Health Care Policy and Research.

Table Graphic Jump Location
Table 1. Exclusion Criteria Applied to the Two Groups Used To Form the Population for Study
* 

Percentages do not always add to 100 due to rounding error.

 

Children with low birth weight were already excluded from CAS cohort at time of recruitment.

Table Graphic Jump Location
Table 2. Distribution of Selected Characteristics by Race for the Two Study Groups Combined for Analysis
* 

Mother, father, or both reported smoking.

Table Graphic Jump Location
Table 3. Asthma Diagnosis, Symptoms, and Airway Responsiveness in a Population of Middle-class Children
* 

Reported symptoms in last 12 months.

Table Graphic Jump Location
Table 4. CCRs by Asthma Diagnosis and Race in a Population of Middle-class Children 6 to 8 Years Old
* 

Mann-Whitney test.

Table Graphic Jump Location
Table 5. Serum IgE by Asthma Diagnosis and Race in a Population of Middle-class Children 6 to 8 Years Old
Figure Jump LinkFigure 1. Relationship of serum IgE and methacholine responsiveness in AA and EA children. AA children are represented by the solid circles and the dashed line. EA children are represented by the plus (+) signs and the solid line.Grahic Jump Location
Table Graphic Jump Location
Table 6. Allergic Status Via Skin Test and Serum-Specific IgE by Race
* 

All AA children and a random sample of 116 EA children were tested for cockroach antigen.

We would like to acknowledge the clinical contributions of Dr. Tonya Corbin to this research.

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Taylor, WR, Newacheck, PW Impact of childhood asthma on health.Pediatrics1992;90,657-662. [PubMed]
 
Weitzman, M, Gortmaker, SL, Sobol, AM, et al Recent trends in the prevalence and severity of childhood asthma.JAMA1992;268,2673-2677. [CrossRef] [PubMed]
 
Hankinson, JL, Kinsley, KB, Wagner, GR Comparison of spirometric reference values for Caucasian and African American blue-collar workers.J Occup Environ Med1996;38,137-143. [CrossRef] [PubMed]
 
Pattemore, PK, Asher, MI, Harrison, AC, et al The inter-relationship among bronchial hyperresponsiveness, the diagnosis of asthma and asthma symptoms.Am Rev Respir Dis1990;143,549-554
 
Grundbacher, FJ, Massie, FS Levels of immunoglobulin G, M, A, and E at various ages in allergic and nonallergic black and white individuals.J Allergy Clin Immunol1985;75,651-658. [CrossRef] [PubMed]
 
Rosenstreich, DL, Eggleston, P, Kattan, M, et al The role of cockroach allergy and exposure to cockroach allergen in causing morbidity among inner-city children with asthma.N Engl J Med1997;336,1356-1363. [CrossRef] [PubMed]
 
Lindberg, RE, Arroyave, C Levels of IgE in serum from normal children and allergic children as measured by an enzyme immunoassay.J Allergy Clin Immunol1986;78,614-618. [CrossRef] [PubMed]
 
Forastiere, F, Corbo, GM, Dell’Orco, V, et al A longitudinal evaluation of bronchial responsiveness to methacholine in children: role of baseline lung function, gender, and change in atopic status.Am J Respir Crit Care Med1996;153,1098-1104. [PubMed]
 
Mochizuki, H, Shigeta, M, Kato, M, et al Age-related changes in bronchial hyperreactivity to methacholine in asthmatic children.Am J Respir Crit Care Med1995;152,906-910. [PubMed]
 
Zhu, BP, Giovino, GA, Mowery, PD, et al The relationship between cigarette smoking and education revisited: implications for categorizing persons’ educational status.Am J Public Health1996;86,1582-1589. [CrossRef] [PubMed]
 
Hadden, WC Annotation: the use of educational attainment as an indicator of socioeconomic position.Am J Public Health1996;86,1525-1526. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. Relationship of serum IgE and methacholine responsiveness in AA and EA children. AA children are represented by the solid circles and the dashed line. EA children are represented by the plus (+) signs and the solid line.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Exclusion Criteria Applied to the Two Groups Used To Form the Population for Study
* 

Percentages do not always add to 100 due to rounding error.

 

Children with low birth weight were already excluded from CAS cohort at time of recruitment.

Table Graphic Jump Location
Table 2. Distribution of Selected Characteristics by Race for the Two Study Groups Combined for Analysis
* 

Mother, father, or both reported smoking.

Table Graphic Jump Location
Table 3. Asthma Diagnosis, Symptoms, and Airway Responsiveness in a Population of Middle-class Children
* 

Reported symptoms in last 12 months.

Table Graphic Jump Location
Table 4. CCRs by Asthma Diagnosis and Race in a Population of Middle-class Children 6 to 8 Years Old
* 

Mann-Whitney test.

Table Graphic Jump Location
Table 5. Serum IgE by Asthma Diagnosis and Race in a Population of Middle-class Children 6 to 8 Years Old
Table Graphic Jump Location
Table 6. Allergic Status Via Skin Test and Serum-Specific IgE by Race
* 

All AA children and a random sample of 116 EA children were tested for cockroach antigen.

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Weitzman, M, Gortmaker, SL, Sobol, AM, et al Recent trends in the prevalence and severity of childhood asthma.JAMA1992;268,2673-2677. [CrossRef] [PubMed]
 
Hankinson, JL, Kinsley, KB, Wagner, GR Comparison of spirometric reference values for Caucasian and African American blue-collar workers.J Occup Environ Med1996;38,137-143. [CrossRef] [PubMed]
 
Pattemore, PK, Asher, MI, Harrison, AC, et al The inter-relationship among bronchial hyperresponsiveness, the diagnosis of asthma and asthma symptoms.Am Rev Respir Dis1990;143,549-554
 
Grundbacher, FJ, Massie, FS Levels of immunoglobulin G, M, A, and E at various ages in allergic and nonallergic black and white individuals.J Allergy Clin Immunol1985;75,651-658. [CrossRef] [PubMed]
 
Rosenstreich, DL, Eggleston, P, Kattan, M, et al The role of cockroach allergy and exposure to cockroach allergen in causing morbidity among inner-city children with asthma.N Engl J Med1997;336,1356-1363. [CrossRef] [PubMed]
 
Lindberg, RE, Arroyave, C Levels of IgE in serum from normal children and allergic children as measured by an enzyme immunoassay.J Allergy Clin Immunol1986;78,614-618. [CrossRef] [PubMed]
 
Forastiere, F, Corbo, GM, Dell’Orco, V, et al A longitudinal evaluation of bronchial responsiveness to methacholine in children: role of baseline lung function, gender, and change in atopic status.Am J Respir Crit Care Med1996;153,1098-1104. [PubMed]
 
Mochizuki, H, Shigeta, M, Kato, M, et al Age-related changes in bronchial hyperreactivity to methacholine in asthmatic children.Am J Respir Crit Care Med1995;152,906-910. [PubMed]
 
Zhu, BP, Giovino, GA, Mowery, PD, et al The relationship between cigarette smoking and education revisited: implications for categorizing persons’ educational status.Am J Public Health1996;86,1582-1589. [CrossRef] [PubMed]
 
Hadden, WC Annotation: the use of educational attainment as an indicator of socioeconomic position.Am J Public Health1996;86,1525-1526. [CrossRef] [PubMed]
 
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